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Erythropoietin—Not at the Olympics but Maybe for Anemic Heart Failure Patients

Erythropoietin increased the exercise duration, peak oxygen consumption, and hemoglobin of patients with anemic heart failure in a study reported in this week’s issue of Circulation (Circulation. 2003;107:294–299) by researchers from the Department of Medicine at Columbia Presbyterian Medical Center in New York.

The drug has been banned from amateur athletics as performance enhancing, but physicians led by Donna Mancini, MD, attempted to determine if it could help patients who have chronic heart failure who are also anemic. In this study, 26 anemic patients aged 57±11 years were randomized to 15 000 to 30 000 IU of erythropoietin or a placebo each week for 3 months.

Twelve patients in the group that received erythropoietin reported feeling improved versus 1 in the placebo group. Hemoglobin increased in the erythropoietin group as did peak oxygen consumption and exercise duration. There was no significant change in the placebo group.

The authors wrote: “Correction of anemia with EPO [erythropoietin] is well tolerated in CHF patients. It increases Hb [hemoglobin] and exercise capacity in these patients. . . . One mechanism of the improvement in Vo2 with EPO therapy is the increased oxygen delivery from increased Hb concentration.”

Statins Have Effect on C-Reactive Protein and Cytomegalovirus

Statins appeared to reduce mortality among patients with coronary artery disease who have evidence of cytomegalovirus infection and high levels of C-reactive protein, according to researchers from the Latter Days Saints Hospital Cardiovascular Department in Salt Lake City, Utah, in a report in this week’s issue of Circulation (Circulation. 2003;107:220–222).

In the study led by Benjamin D. Horne, MPH, and Joseph B. Muhlestein, MD, researchers monitored the course of 2315 patients with significant coronary artery disease for an average of 2.4 years. Levels of antibodies to cytomegalovirus and concentration of C-reactive protein were measured at baseline and the statin prescription was recorded. The researchers found that statins reduced mortality in individuals with increased levels of C-reactive protein and evidence of cytomegalovirus infection.

The authors noted: “This is the first study to report a benefit of statin therapy on infection-associated clinical events: statins reduced the increased mortality associated with CMV [cytomegalovirus] seropositivity. This benefit was independent of CRP but also reduced CRP-associated mortality rates. These results support the concept that statins exert non–lipid-lowering effects on CAD [coronary artery disease] risk, including anti-inflammatory properties. Uniquely, they also suggest that these effects extend beyond those associated with CRP [C-reactive protein].”

Chilled Platelets—Why They Don’t Work

Researchers from the Brigham and Women’s Hospital in Boston, Mass, report in the January 10, 2003, issue of Cell (Cell. 2003;112:87–97) that they think they have discovered why refrigerated platelets rapidly disappear from circulation. The phenomenon limits the use of these life-saving blood products because their room-temperature shelf life is particularly short.

In the study, Karin Hoffmeister, MD, and her colleagues report that von Willebrand factor receptors, which are usually spread throughout the platelet surface, aggregate in clusters when blood is chilled. According to the researchers, the clusters of von Willebrand factor receptors activated a surface receptor called CR3 found on white blood cells to recognize and remove the platelets.

If chilled platelets were transfused in mice bred to lack CR3, they no longer disappeared from circulation and function normally. This means that the change in the configuration of the von Willebrand factor receptor did not affect the platelets’ ability to aid clotting.

“This finding suggests that a modification of the platelet receptor might permit chilled platelets to circulate with retention of normal function. Refrigeration of platelets could significantly impact platelet transfusion technology by increasing available platelet supplies,” said Thomas P. Stossel, MD, one of the study’s authors, in a released statement.

Genetics of Familial Atrial Fibrillation

A family with a rare, inherited form of atrial fibrillation helped scientists from China and France identify the gene that causes the disease, the researchers reported in the January 10, 2003, issue of the journal Science (Science. 2003;299:251–254).

The gene in question is KCNQ1 on chromosome 11 that encodes a protein subunit of an ion channel that controls the movement of potassium through the cell membrane. The researchers, led by Yi-Han Chen, MD, of Tongji University in Shanghai, China, and Shi-Jie Xu, MD, of the Chinese National Human Genome Center in Shanghai, studied a large, four-generation family in China, which included 44 living members from rural villages and cities in the northern Shandong Province. Of these, 16 had atrial fibrillation, all of which was hereditary.

They found that there was a nucleotide substitution in the KCNQ1 gene in all the affected families members but not in those who did not have atrial fibrillation. The researchers confirmed that the genetic disruption affected the function of the KCNQ1 potassium channel. KCNQ1 had previously been linked to familial ventricular fibrillation and long-QT syndrome, but in that case, the change led to a loss of the ability of the channel to transmit potassium. In the case of the familial atrial fibrillation, the change increased function of the potassium channel.

“The mutation in KCNQ1 causes a marked enhancement of its function, tips the normal balance of the process, and renders the cardiac myocytes more susceptible to atrial fibrillation,” Drs Chen and Xu said in a released statement.